tbuckley/cabot-search huggingface dataset:
AB0766 STEP-DOWN TREATMENT WITH MEPOLIZUMAB FOR EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (EGPA). REAL-LIFE EXPERIENCE OF A SINGLE-CENTER COHORT
Authors: V. Batani, B. N. Germinario, M. Lanzillotta, A. Cariddi, L. Moroni, L. Dagna
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Mepolizumab is an anti-interleukin-5 (IL-5) agent approved for EGPA at the dose of 300 mg every 4 weeks. However, from real-life studies, evidence is accruing of its comparable effectiveness at "asthma-dose" of 100 mg every 4 weeks. The preferred approach at our center is to start mepolizumab 300 mg/4 weeks and to reduce to 100 mg/4 weeks once remission is achieved (Birmingham Vasculitis Activity Score - BVAS=0), asthma is controlled (Asthma Control Test – ACT &gt;20), eosinophil count is normalized and glucocorticoids are withdrawn (step-down approach). <h3>Objectives</h3> To assess the long term-efficacy of step-down treatment with mepolizumab in EGPA. <h3>Methods</h3> We reviewed medical charts of patients with EGPA treated with mepolizumab from April 2014 to December 2022. We divided patients by homogeneous dosing schedule and compared disease activity and characteristics at baseline and over time. <h3>Results</h3> We treated 38 patients for a median follow up of 38 months (IQR 29-53). Seven patients underwent a step-up approach (starting with mepolizumab 100 mg/4w and subsequent switching to mepolizumab 300 mg/4w in case of failure). Among them, only 1 patient (17%) needed a dose increase due to uncontrolled respiratory symptoms. Mepolizumab 300 mg/4w was started in 31 patients allowing a step-down in 9 (29%), without any patient having to increase the dose again. Both subgroups of the step-down strategy showed significant reduction in terms of BVAS, ACT, serum eosinophils and daily prednisone dose at last follow-up. At the same time presented a high proportion of nasal exacerbations (33 vs. 9% p=0.31). [Table 1] <h3>Conclusion</h3> In our experience, a step-down approach with mepolizumab in EGPA is reasonable and allows to safely reach the low-dose regimen in a great proportion of patients. Nasal polyps are the new challenge for physicians treating EGPA in an age where a steroid-free remission is an achievable target. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB1629 PREVALENCE OF MUSCULOSKELETAL AND WIDESPREAD PAIN IN A REPRESENTATIVE COHORT OF THE FRENCH GENERAL POPULATION
Authors: F. Bailly, A. Petit, S. Kab, V. Foltz, M. Badard, B. Fautrel
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Few studies include a sufficient number of people to be representative of a general population and to estimate the musculoskeletal pain prevalence. <h3>Objectives</h3> To estimate the prevalence of musculoskeletal and widespread pain in the French popualtion using a large and representative cohort. <h3>Methods</h3> The Constances cohort is composed of volunteers, aged 18 to 69 years at inclusion. Eligible subjects were selected at random by stratified sampling with unequal probabilities, over-representing individuals with a higher probability of not volunteering (according to their age, sex, socioprofessional category) with adjustment coefficients weight participation bias. Individuals diagnosed with a cancer were excluded. Musculoskeletal pain was assessed by the Nordic Questionnaire. Significant pain lasted at least 30 days during the last 12 months. Widespread pain concerned at least 4 of the 6 areas. Chronic moderate to severe pain reached a pain score ≥ 4/10 in the last 7 days. Data from the entire cohort were described and then the French population prevalence was estimated, based on people included in 2017 with adjustment coefficients. <h3>Results</h3> 193,436 people were included in the cohort. The French population prevalence of each pain location and widespread pain were estimated among the 25,472 people included in 2017. <h3>Conclusion</h3> The prevalence of musculoskeletal pain in the French population is high, particularly for chronic pain of moderate to severe intensity, which underlines the need to improve their detection, prevention and management. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0703 TOWARDS TREAT-TO-TARGET PATIENT CENTRED CARE: DEVELOPMENT OF MULTIDIMENSIONAL DISEASE SPECIFIC PATIENT REPORTED OUTCOME MEASURES QUESTIONNAIRE FOR GIANT CELL ARTERITIS
Authors: Y. El Miedany, D. Palmer, M. Toth, M. Elgaafary, S. Bahlas, S. A. Mahran, M. H. Abu-Zaid, W. Hassan, W. Elwakil
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Giant Cell Arteritis (GCA) is the commonest form of systemic vasculitis in people over the age of 50. In 2017, the OMERACT Vasculitis Working Group published a core set of domains and outcome measures for use in clinical trials in large vessel vasculitis [1] and highlighted the lack of a disease-specific patient reported outcomes (PROMs) for GCA. The OMERACT group proposed a draft core set of domains for GCA, including disease specific domains, organ and arterial function, psychosocial impact and physical function biomarkers, fatigue, pain, as well as death. <h3>Objectives</h3> To assess the validity, reliability and responsiveness to change of a patient self-reported questionnaire to assess for the construct outcome measures, co-morbidities and the impact of GCA and its treatment on health-related quality of life in GCA patients. <h3>Methods</h3> The PROMs-GCA was conceptualized based on frameworks used by the WHO Quality of Life tool and the PROMIS. Initially, cognitive interviews were conducted to identify item pool of questions. Item selection and reduction was achieved based on patients as well as an interdisciplinary group of specialists. Rasch and internal consistency reliability analyses were implemented. The questionnaire included the GCA specific physical and psychological symptoms, sense of self, symptoms severity using numerical visual analogue scale (0-10) in addition to assessment of functional disability, quality of life (QoL), review of the systems, glucocorticoids benefit:risks, comorbidities as well as motivation [2]. In addition, every patient completed HAQ and EQ-5D questionnaires. <h3>Results</h3> A total of 52 GCA patients completed the questionnaire. The PROMs-GCA questionnaire was reliable as demonstrated by a high standardized alpha (0.867-0.941). Content construct assessment of the PROMs-GCA/functional disability and QoL revealed significant correlation (p&lt; 0.01) with both HAQ and EQ-5D. Changes in functional disability, QoL showed significant (p&lt; 0.01) variation with diseases activity status in response to therapy. <h3>Conclusion</h3> The developed PROMs-GCA questionnaire is a reliable and valid instrument for assessment of patients living with GCA. A phased treatment regimen depending on the severity of GCA as well as the patient's preferences and comorbidities are the best approach to tailored patient management. <h3>References</h3> [1]Sreih AG, et al. Development of a core set of outcome measures for large-vessel vasculitis: report from OMERACT 2016. J Rheumatol. 2017;44(12):1933–7 [2]El Miedany et al. Meaningful patient engagement in inflammatory arthritis: Development of the patient motivation questionnaire. Clin Rheumatol. 2017 doi: 10.1007/s10067-017-3605-x. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0425 REAL-WORLD EFFECTIVENESS OF FILGOTINIB IN BELGIAN PATIENTS WITH RHEUMATOID ARTHRITIS
Authors: D. C. Diederik, P. Durez, J. Lenaerts, R. Westhovens, P. Verschueren
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Filgotinib (FIL), a preferential Janus Kinase (JAK) inhibitor targeting the JAK1 enzyme, has demonstrated efficacy in rheumatoid arthritis (RA) in clinical trials. FIL is reimbursed in Belgium since August 2021 for adult patients with moderate to severe RA with a DAS28 score &gt;3.7 and inadequate response or intolerance to 2 conventional DMARDs including Methotrexate. Today, limited data exist on the real-world effectiveness of FIL in RA. <h3>Objectives</h3> Our aim was to examine the short-term effectiveness of FIL in a heterogeneous RA population. <h3>Methods</h3> Patients were included from the electronic platform "Tool for Administrative Reimbursement Drug Information Sharing" (TARDIS). Data from all Belgian RA patients on biologic and targeted therapy are collected in this platform during the submission of a request for initiation or prolongation of reimbursement of these drugs. The study population included adult patients ≥18 years starting FIL between August 2021 and November 2022. Baseline characteristics (demographics, clinical characteristics, treatment history) of Belgian RA patients treated with FIL were registered. Effectiveness of FIL was determined by the patient proportion achieving remission (DAS28 &lt;2.6), low disease activity (DAS28 ≤3.2), HAQ-DI≤0.25 (HAQ25) and minimum HAQ-DI-decrease (MCID_HAQ) since baseline of 0.22, at the first follow-up moment, structurally planned in TARDIS after 3 months. Sensitivity analyses were performed in patients starting FIL as 1st, 2nd or 3th+-line advanced therapy. <h3>Results</h3> In total, 405 RA patients on FIL were included, representing all newly initiated FIL patients. Table 1 gives detailed information on the demographics, clinical characteristics and treatment history. Of the 228 patients with information on treatment at the next follow-up moment, 210 (92%) continued FIL, and 6 (3%), 9 (4%), and 3 (1%) changed to a TNFi, non-TNFi and JAKi respectively. In total, 193/405 (48%) patients could be included in the effectiveness analysis. Remission and low disease activity were reached in 61% (117/193) and 81% (156/193) of patients respectively. Baseline mean ±SD DAS28 was 4.9 ±0.8. The DAS28 change was 2.5 ±1.2, resulting in a mean ±SD DAS28 of 2.4 ±1.1 at first follow-up. HAQ25 and MCID_HAQ were reached in 21% (41/193) and 70% (136/193) of patients. FIL efficacy slightly decreased with increasing line of therapy (Figure 1). <h3>Conclusion</h3> FIL treatment offered promising clinical outcomes after 3 months in most patients with moderately to severely active RA in a real-world setting. <h3>Acknowledgements</h3> on behalf of the Royal Belgian Society for Rheumatology. This work was financially supported by Galapagos. <h3>Disclosure of Interests</h3> None Declared.
POS1440 EVIDENCE FOR INCREASED RESPONSIVENESS TO INTERFERON TYPE I IN CD8+ T CELLS IN PATIENTS WITH GIANT CELL ARTERITIS
Authors: M. Van Nieuwland, I. Esen, R. Reitsema, W. Abdulahad, Y. Van Sleen, M. Sandovici, E. Brouwer, L. Van Bon
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Giant cell arteritis (GCA) is a vasculitis which can lead to severe complications when not timely recognized and treated. There is a need for the discovery of biomarkers to expedite the diagnostic process. Interferon type I (IFN-I) is increasingly recognized as a key player in a range of autoimmune diseases and might play a role in GCA pathogenesis [1]. However, evidence for IFN-I potentially linking innate and adaptive immune responses in GCA is limited. IFN-I activates the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway, leading to an increased expression of interferon stimulated genes (ISGs). <h3>Objectives</h3> In this study, IFN-I involvement in GCA pathogenesis is explored. <h3>Methods</h3> Phopho-STAT1 (pSTAT1) expression was investigated in IFN-α-stimulated peripheral mononuclear cells (PBMCs) gated separately for CD8+ T-cells of patients with GCA (n=18), healthy controls (HC, n=15) and infection controls (n=11) by fluorescent cell barcoding and flow cytometry. Also, in 3 GCA patients and 3 HCs, single cell RNA sequencing was performed on PBMCs focusing on ISG expression. Furthermore, IFN-I induced myxovirus-resistance protein A (MxA) and CD8+ expression was investigated in temporal artery biopsies (TAB) of GCA patients (n=20) and GCA mimics (n=20) by immunohistochemistry. <h3>Results</h3> pSTAT1 expression was increased in IFN-α stimulated CD8+ T-cells from patients with GCA compared to both HC (p&lt;0.05) and infection controls. Furthermore, Interferon Induced Transmembrane Protein 1 (IFITM1) mRNA expression was upregulated in peripheral blood CD8+ T cells (p&lt;0.001). MxA was present in TABs of 13/20 GCA patients compared to 2/20 mimics and MxA location co-localized with CD8+ expression in the tissue. <h3>Conclusion</h3> Our results provide evidence for IFN-I involvement in GCA pathogenesis, with CD8+ T cells as IFN-I responding effector cells. Increased pSTAT1, IFITM1 and MxA expression may reflect increased IFN-I responsiveness in CD8+ T-cells of GCA patients, both locally and systemically. These findings warrant further investigation regarding IFN-I induced biomarkers and IFN-I related novel therapeutic options. <h3>Reference</h3> [1]Nordborg C, Larsson K, Aman P, Nordborg E. Expression of the class I interferon-related MxA protein in temporal arteries in polymyalgia rheumatica and temporal arteritis. Scand J Rheumatol. 2009 Mar-Apr;38(2):144-8. doi: 10.1080/03009740802448841. PMID: 19177264. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0044 INTERLEUKIN-18 BINDING PROTEIN REGULATES THE APOPTOSIS AND NECROPTOSIS OF FIBROBLAST-LIKE SYNOVIOCYTES AND CHONDROCYTES IN RHEUMATOID ARTHRITIS
Authors: S. H. Lee, H. K. Min, H. R. Kim
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Interleukin (IL)-18 plays a pro-inflammatory role in rheumatoid arthritis (RA), and its decoy receptor IL-18 binding protein (IL-18BP) has a potential therapeutic role. <h3>Objectives</h3> We investigated the role of IL-18BP on the joint destruction process of RA by accessing the effects of IL-18BP on fibroblast-like synoviocytes (FLSs) and chondrocytes. <h3>Methods</h3> Peripheral blood mononuclear cells (PBMCs) from patients with RA and healthy controls were cultured under T cell proliferative conditions with 10, 50, or 100 ng/mL of IL-18BP. After three days of culture, flow cytometry for CD4+ T cells was performed using various IL-18BP concentrations. The apoptosis and necroptosis of FLSs and chondrocytes were measured by flow cytometry using annexin V and propidium iodide (PI) and western blot under TNF-α stimulation with IL-18BP (10, 50, and 100 ng/mL). <h3>Results</h3> Differentiation of CD4+ IL-17A+ and CD4+ IL-4+ cells decreased and that of CD4+ CD25high Foxp3+ and CD4+ interferon (IFN)-γ+ cells increased on addition of IL-18BP to cultured RA patient-driven PBMCs. RA-FLS migration ability was not suppressed by IL-18BP after 12 or 24 h. IL-18BP increased annexin V+ FLS level and reduced annexin V+ chondrocyte level in a dose-dependent manner, whereas PI+ annexin V- FLS and chondrocyte levels were suppressed by 50, 100 ng/mL IL-18BP in culture. <h3>Conclusion</h3> The administration of IL-18BP regulated the type 17 helper T cell/ regulatory T cell imbalance and attenuated the production of pro-inflammatory cytokines. IL-18BP further increased FLS apoptosis and decreased the necroptosis of FLS/chondrocytes and apoptosis of chondrocytes suggesting the joint preservative potential of IL-18BP. <h3>References</h3> [1]BERTHELOOT D, LATZ E, FRANKLIN BS: Necroptosis, pyroptosis and apoptosis: an intricate game of cell death. Cell Mol Immunol 2021; 18: 1106-21. [2]MIN HK, KIM S, LEE JY, KIM KW, LEE SH, KIM HR: IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell/ regulatory T cell imbalance in rheumatoid arthritis. J Transl Med 2021; 19: 392. [3]SHAO XT, FENG L, GU LJ et al.: Expression of interleukin-18, IL-18BP, and IL-18R in serum, synovial fluid, and synovial tissue in patients with rheumatoid arthritis. Clin Exp Med 2009; 9: 215-21. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0575 IMPACT OF PATIENT-REPORTED DISEASE ACTIVITY ON HEALTH-RELATED QUALITY OF LIFE (HRQoL) IN SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) PATIENTS. DATA FROM THE ALMENARA LUPUS COHORT
Authors: M. F. Ugarte-Gil, R. V. Gamboa Cárdenas, V. Pimentel-Quiroz, C. Reategui Sokolova, C. Elera-Fitzcarrald, J. Alfaro Lozano, C. Pastor Asurza, Z. Rodriguez Bellido, R. Perich Campos, G. S. Alarcon
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Health-related quality of life (HRQoL) is impaired in systemic lupus erythematosus (SLE) patients, but its association with physicians reported disease activity is modest to none. <h3>Objectives</h3> To determine the impact of patients reported disease activity on their HRQoL. <h3>Methods</h3> We evaluated patient-reported disease activity on SLE patients from the Almenara Lupus Cohort. Disease activity was assessed using the Lupus Foundation of America Rapid Evaluation of Activity in Lupus (LFA-REAL) patient-reported outcome (PRO) which ranges between 0 and 1200 (the higher the score is, the worse the activity is); HRQoL was ascertained using the LupusQoL which ranges between 0 and 100 (the higher the score is, the better the HRQoL). Generalized estimating equations were performed for each domain of the LupusQoL and the LFA-REAL PRO measured at the previous visit; multivariable models were adjusted for possible confounders (age at diagnosis, gender, educational level, disease duration, SLEDAI-2K, SDI, prednisone dose, antimalarials and immunosuppressive drug use and the same domain of LupusQoL) measured at the same visit as the LFA-REAL PRO. B was reported per 10 units increase of the LFA-REAL PRO. <h3>Results</h3> A total of 259 patients and 582 visits were included. Mean (SD) LFA-REAL PRO was 242.91 (178.92). The most affected LupusQoL domains at baseline were burden to others 57.5 (SD 31.5), intimate relationship 64.1 (SD 33.1) and body image 62.6 (SD 30.7). LFA-REAL PRO predicted a worse HRQoL in all domains, even after adjustment by possible confounders (Table 1). <h3>Conclusion</h3> A higher patient-reported disease activity predicted a worse HRQoL in SLE patients, even after adjustment for possible confounders. Strategies to improve how the patients feel and manage their disease could be useful to improve their HRQoL. Patient-reported disease activity should be included in the evaluation of SLE patients on a regular basis. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> Manuel F. Ugarte-Gil Speakers bureau: GSK, Consultant of: Aztra Zeneca, Grant/research support from: Janssen, Rocío Violeta Gamboa Cárdenas: None declared, Victor Pimentel-Quiroz: None declared, Cristina Reategui Sokolova: None declared, Claudia Elera-Fitzcarrald: None declared, Jose Alfaro Lozano: None declared, Cesar Pastor Asurza: None declared, Zoila Rodriguez Bellido: None declared, Risto Perich Campos: None declared, Graciela S Alarcon: None declared.
AB1061 CORRELATION OF SERUM SUBFATIN, CTHRC1, CTRP3, CTRP6 LEVELS WITH DISEASE ACTIVITY IN PATIENTS WITH AXIAL SPONDYLOARTHRITIS
Authors: İ. M. Baytaroğlu Uçar, G. Sargin, A. Tuzcu, S. Cildag, T. Senturk
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> It has been determined that biological treatments affect the serum concentration of these biomarkers independently of disease activity. As current adipokines and known modulators of inflammation, it may play a role in evaluating the efficacy of treatment, especially in cases using biologic agents. <h3>Objectives</h3> To analyze novel biomarkers from the C1q TNF superfamily and their function in autoimmune inflammatory rheumatic disorders, as well as to look for a biomarker capable of evaluating both the clinical disease activity and aiding in the evaluation of therapy efficacy. <h3>Methods</h3> Sixty-one AxSpa patients and 30 healthy controls were enrolled in the study. Serum biomarkers subfatin, CTHRC1, CTRP3, CTRP6, IL-6, IL-17, TNF-α and disease activity indexes BASDAI, BASFI, MASES, ASDAS-ESR/CRP were evaluated and compared. Patients were then classified, and their serum biomarkers were also assessed according to their disease activity scores, and further according to their treatment regimens. <h3>Results</h3> None of the examined biomarkers revealed a discernible difference between patients and healthy controls. Although the difference was not statistically significant, healthy controls were found to have lower median concentrations of serum subfatin, CTHRC1, CTRP3, CTRP6, IL-6, IL-17, and TNF-α. Furthermore, no association between the research biomarkers and clinical disease activity was seen once the patients were categorized according to the severity of their disease. Finally, it was discovered that biological therapies had an impact on these biomarkers' serum concentrations (Table 1) regardless of the disease's activity. <h3>Conclusion</h3> Circulating levels of subfatin, CTHRC1, CTRP3, CTRP6, IL-6, IL-17, and TNF-α, which are novel adipokines and well-known inflammatory mediators, may be important for determining treatment effectiveness, particularly in patients receiving biologics. We were unable to prove a connection between serum biomarker levels and clinical disease activity, though. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0930 THE VALUE OF THE CURRENT DIAGNOSTIC TOOLS IN THE DIAGNOSIS OF INFLAMMATORY MYOPATHIES: A MULTICENTRE STUDY
Authors: E. Kaltsonoudis, E. Pelechas, T. Zoi, M. Migkos, T. Dimitroulas, N. Kougkas, A. Drosos, P. Voulgari
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> traditionally, the diagnosis of inflammatory myopathies has been based on clinical signs and symptoms (muscle weakness and characteristic skin involvement, especially in dermatomyositis), increased muscle enzymes, electromyographic findings, skin or muscle biopsy, as well as anti-Jo1 antibodies (antisynthetase syndrome). However, this approach has led to significant diagnostic gaps in atypical cases such as in those of pure lung involvement. <h3>Objectives</h3> to evaluate the diagnostic yield of each procedure in a sample of 61 patients who were diagnosed, followed-up and treated in two tertiary university rheumatology clinics in Greece. <h3>Methods</h3> serum samples tested using a myositis panel (Mi-2α, Mi-2β, Ku, PM-Scl100, PM-Scl 75, SRP, Jo-1, PL-7, PL-12, OJ, EJ, Ro-52, TIF1γ, MDA5, NXP2, SAE1) and muscle enzymes (CK, aldolase, LDH, SGOT, SGPT). Electromyography has been carried out in all patients, whereas in 27 with elevated muscle enzymes or muscle weakness an MRI-guided muscle biopsy has been done. In addition, in 8 patients, a skin biopsy has been performed and in all patients a detailed examination (determination of muscle strength) has been performed in all muscle groups. <h3>Results</h3> in 42 cases the diagnosis has been made after a positive myositis panel, while in 20 cases there was also a histological confirmation. In 8 cases, the diagnosis has been made on the grounds of positive clinical features and characteristic findings on the electromyogram. Only 4 patients have been diagnosed on the basis of histological findings in the absence of other laboratory and clinical findings <b>(table 1</b>). The most common autoantibodies in patients with lung involvement were Jo-1, PL-12 and PL-7. <h3>Conclusion</h3> based on the aforementioned results, a myositis panel seems a reasonable and reliable diagnostic strategy as it improves significantly the diagnostic yield of an inflammatory myopathy. In addition, it gives a diagnostic "alibi" for the therapeutic approaches that otherwise can be administered only by histological confirmation. Finally, in patients with atypical signs and symptoms such as lung fibrosis that cannot be attributed elsewhere, a myositis panel should be performed. <h3>Reference</h3> [1]Tsamis KI, Boutsoras C, Kaltsonoudis E, Pelechas E, Nikas IP, Simos YV, et al. Clinical features and diagnostic tools in idiopathic inflammatory myopathies. Crit Rev Clin Lab Sci. 2022;59:219-240. Doi: 10.1080/10408363.2021.2000584 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.